COARTEM (artemether/lumefantrine)
ANTIMALARIAL DRUGS·PLASMODIUM FALCIPARUM MALARIA·+1
Novartis Pharmaceuticals
Indication
Chloroquine-resistant Plasmodium falciparum malaria
Chloroquine-resistant *Plasmodium falciparum* malaria is an acute, potentially life-threatening parasitic bloodstream infection caused by *Plasmodium falciparum* strains that survive therapeutic concentrations of the standard 4-aminoquinoline agent chloroquine. Read more about Chloroquine-resistant Plasmodium falciparum malaria
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Coming soonChloroquine-resistant *Plasmodium falciparum* malaria is an acute, potentially life-threatening parasitic bloodstream infection caused by *Plasmodium falciparum* strains that survive therapeutic concentrations of the standard 4-aminoquinoline agent chloroquine.
Transmitted by the bite of infective female *Anopheles* mosquitoes, the protozoan invades and destroys host erythrocytes, with resistance pathophysiologically driven primarily by point mutations in the parasite's *pfcrt* gene that reduce chloroquine accumulation within its digestive vacuole.
Patients classically present with paroxysmal fevers, chills, diaphoresis, severe hemolytic anemia, and splenomegaly.
Due to extensive cytoadherence and microvascular sequestration, the infection carries a high risk of rapidly deteriorating into severe malaria, characterized by cerebral malaria, metabolic acidosis, pulmonary edema, and multi-organ dysfunction.
- cdc.gov
Chloroquine-resistant *Plasmodium falciparum* malaria is an acute, potentially life-threatening parasitic bloodstream infection caused by *Plasmodium falciparum* strains that survive therapeutic concentrations of the standard 4-aminoquinoline agent chloroquine
- oup.com
Chloroquine-resistant *Plasmodium falciparum* malaria is an acute, potentially life-threatening parasitic bloodstream infection caused by *Plasmodium falciparum* strains that survive therapeutic concentrations of the standard 4-aminoquinoline agent chloroquine
- cdc.gov
Transmitted by the bite of infective female *Anopheles* mosquitoes, the protozoan invades and destroys host erythrocytes, with resistance pathophysiologically driven primarily by point mutations in the parasite's *pfcrt* gene that reduce chloroquine accumulation within its digestive vacuole
- nih.gov
Transmitted by the bite of infective female *Anopheles* mosquitoes, the protozoan invades and destroys host erythrocytes, with resistance pathophysiologically driven primarily by point mutations in the parasite's *pfcrt* gene that reduce chloroquine accumulation within its digestive vacuole
- plos.org
Transmitted by the bite of infective female *Anopheles* mosquitoes, the protozoan invades and destroys host erythrocytes, with resistance pathophysiologically driven primarily by point mutations in the parasite's *pfcrt* gene that reduce chloroquine accumulation within its digestive vacuole
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